FIELD OF THE INVENTION
The present invention relates to implantable medical devices and methods, and more particularly to a dual-chamber implantable pacemaker or pacemaker system having an improved upper rate response adapted to synchronize the atrium of a patient's heart with the ventricle for a higher percentage of the time, thereby enhancing the upper rate cardiac output.
The basic function of the heart is to pump (circulate) blood throughout the body. The blood serves as a medium for delivering oxygen and nutrients to the various tissues while removing waste products and carbon dioxide. The heart is divided into four chambers comprised of two atria and two ventricles. The atria are the collecting chambers holding the blood which returns to the heart until the ventricles are ready to receive this blood. The ventricles are the primary pumping chambers. The pumping function of the heart is achieved by a coordinated contraction of the muscular walls of the atria and the ventricles.
The atria are more than simple collecting chambers. The atria contain the heart's own (natural, native or intrinsic) pacemaker that controls the rate at which the heartbeats or contracts. In addition, the atrial contraction helps to fill the ventricle, further contributing to optimal filling and thus maximizing the amount of blood which the heart is able to pump with each contraction. Thus, atrial contraction is followed after a short period of time (normally 120 to 200 ms) by ventricular contraction.
The period of cardiac contraction during which the heart actively ejects the blood into the arterial blood vessels is called systole. The period of cardiac relaxation during which the chambers are being filled with blood is called diastole. Atrial and ventricular systole are sequenced allowing the atrial contraction to help optimally fill the ventricle. This is termed AV synchrony.
A cardiac cycle comprises one sequence of systole and diastole. It can be detected by counting the patient's pulse rate. It is also reflected by the cardiac rhythm as recorded by an electrocardiogram (ECG) or electrogram (EGM). The ECG is a recording of the electrical activity of the heart as seen using surface electrodes placed on the surface of the body. The EGM is a recording of the electrical activity of the heart as seen using electrodes placed within the heart. The electrical activity refers to the cardiac depolarization in either the atrium and/or ventricle. In general, on the ECG or EGM, the atrial depolarization is represented by a P-wave, while the ventricular depolarization is represented by a QRS complex, usually abbreviated as an "R-wave". The electrical depolarization triggers or initiates the active muscular contraction. Once the cardiac cells are depolarized, they must repolarize in order for the next depolarization and contraction to occur. Ventricular repolarization is represented by the T-wave. Atrial repolarization is rarely seen on an ECG or EGM as it occurs at virtually the same time as the R-wave, and is thus hidden by this large electrical signal.
A normal heart rate varies between 60 to 100 beats per minute (bpm) with an average of 72 bpm resulting in approximately 100,000 heartbeats per day.
The amount of blood that the heart pumps in one minute is called the cardiac output. It is calculated by the amount of blood ejected with each heartbeat (stroke volume) multiplied by the number of heartbeats in a minute. If the heart rate is too slow to meet the physiologic requirements of the body, the cardiac output will not be sufficient to meet the metabolic demands of the body. Too slow of a heart rate, termed a bradycardia, may thus result in one of two major symptoms: (1) if the heart effectively stops with no heartbeat, there will be no blood flow and if this is sustained for a critical period of time (10 to 30 seconds), the individual will faint; or (2) if there is a heartbeat but it is too slow, the patient will be tired and weak (termed low cardiac output).
A pacemaker is a medical device that is used to selectively stimulate the heart with electrical stimulation pulses aimed at assisting it to perform its function as a pump. Normally, the stimulation pulses are timed to keep the heart rate above a prescribed limit, i.e., to treat a bradycardia. A pacemaker may thus be considered as a pacing system. The pacing system is comprised of two major components. One component is a pulse generator which generates the stimulation pulse and includes the electronic circuitry and the power cell or battery. The other is the lead or leads which electrically couple the pacemaker to the heart.
The pacemaker delivers an electrical stimulus to the heart to cause the heart to contract when the patient's own intrinsic rhythm fails. To this end, pacemakers include sensing circuits that sense the EGM, and in particular that sense the P-waves and/or R-waves in the EGM. By monitoring such P-waves and/or R-waves, the pacemaker circuits are able to determine the intrinsic rhythm of the heart, and provide stimulation pulses that force atrial and/or ventricular depolarization at appropriate times in the cardiac cycle so as to help stabilize the electrical rhythm of the heart.
Pacemakers are described as either single-chamber or dual-chamber systems. A single-chamber system stimulates and senses the same chamber of the heart (atrium or ventricle). A dual-chamber system stimulates and/or senses in both chambers of the heart (atrium and ventricle). Dual-chamber systems may typically be programmed to operate in either a dual-chamber mode or a single-chamber mode.
A three letter code (sometimes expanded to a four or five letter code) is used to describe the basic mode in which the pacemaker is operating. The first three letters refer specifically to electrical stimulation for the treatment of bradycardia, with the first letter indicating the chamber(s) of the heart where the electrical stimulus is delivered (A=atrium; V=ventricle; D=dual or both), the second letter identifying the chamber(s) in which sensing occurs, and the third letter identifying the way a pacemaker responds to a sensed signal (I=inhibited; T=trigger; D=dual or both sensing responses). A fourth position (when used) identifies the degree of programmability and rate modulation, and a fifth position (when used) refers to electrical stimulation therapy for the primary treatment of fast heart rhythms or tachyarrhythmias or tachycardias.
A popular mode of operation for dual-chamber pacemakers is the DDD mode. Specifically, DDD systems provide atrial pacing during atrial bradycardia, ventricular pacing during ventricular bradycardia, and atrial and ventricular pacing during combined atrial and ventricular bradycardia. In addition, DDD systems provide an atrial synchronous mode. Such features more closely approximate the normal response to exercise, or other physiological activity demanding a faster heart rate, by permitting a rate increase to occur commensurate with the rate of the sensed P-wave. This advantageously increases cardiac output and facilitates maintenance of AV synchrony.
Most implantable pacemakers also include some type of upper rate limiting feature to prevent the pacemaker from providing stimulation pulses at a rate that exceeds a prescribed upper rate limit. Such upper rate limit is usually referred to as a "Maximum Tracking Rate", or MTR. The response to upper rate limiting is commonly referred to as Pacemaker Mediated "Wenkebach" Phenomenon.
When Pacemaker Mediated "Wenkebach" Phenomenon occurs, two major consequences usually result. First, when the atrial rate exceeds the MTR, then the PV interval may be prolonged to prevent stimulation at rates exceeding the MTR. The effect is a prolonging of the A-V interval, or the interval between atrial activity and ventricular activity. Second, a P-wave may occasionally occur during the post ventricular atrial refractory period (PVARP), which period immediately follows a V-pulse. P-waves that occur during PVARP are ignored. Hence, it is necessary to wait for the next P-wave to occur before a V-pulse is triggered after a PV interval. The effect is a prolongation of the V-to-V interval to an interval that is longer than the MTR interval (MTRI), where the MTRI=1/MTR when the MTR is expressed in cardiac cycles per second. Either effect above is hemodynamically deleterious. That is, the consequence of a prolonged A-V interval is that the cardiac output decreases because of loss of proper timing of the "atrial kick". Moreover, the occasional prolonging of the V-to-V interval results in the average heart rate being less than the rate available at the MTR. Further, at very high atrial rates or when PVARP is relatively long, the upper rate behavior appears as a 2:1 or higher block (i.e., every other, or every nth, P-wave is blocked by PVARP and is thus not recognized). The consequence is a ventricular rate that is usually 1/2 of the atrial rate. Such a low ventricular rate, even though the "atrial kick" remains intact (at least one-half of the time), can also be very deleterious hemodynamically. In addition, if the unsensed P-wave occurs during systole, then mitral or tricuspid regurgitation may occur. Such regurgitation further degrades hemodynamic performance.
In addition to the above-described degradation of hemodynamic performance caused by prolongation of the PV interval, a prolongation of the PV interval also problematically affects the electrophysiologic performance of the pacemaker/cardiac system. That is, a prolongation of the PV interval enhances the probability of retrograde conduction, as does the upper rate limiting provided by Wenkebach performance. Retrograde conduction, in turn, leads to a much greater susceptibility to a pacemaker mediated tachycardia (PMT). What is needed, therefore, is an improved upper rate performance that does not require the PV interval to be lengthened, but rather preserves the PV interval at a fixed value, thereby reducing the likelihood of retrograde conduction, and minimizing the susceptibility of the pacemaker/cardiac system to a PMT.
The present invention advantageously addresses the above and other needs.